Fig. 2. PHI ameliorated the experimental symptoms in DSS-induced
murine acute UC. (A) DSS-induced murine model. (B) Body weight change
(% initial body weight), diarrhea, stool bleeding, and disease activity
index (DAI). (C) Representative images of colon morphology, quantitative
colon length, and the spleen coefficient. (D) Representative images of
H&E, PAS-Alcian blue staining of colon sections, and histological
scores, bar = 100 μm. (E) Fluorescence intensity of FITC-dextran in
serum. (F) The mRNA and protein levels of tight junction proteins in the
intestine. Compared with the model control group *p <0.05,
**p <0.01, ***p <0.001, n = 6-8.
PHI ameliorated
TNBS-induced murine ulcerative colitis
To better explore the effect of PHI on inflammatory bowel disease, we
also used TNBS-induced mouse model. Used 2.5% TNBS to cause gut
inflammation. Mice were treated with 40 mg/kg PHI from day 0 to the
endpoint (Fig. 3A). Similarly, PHI significantly improved the survival
rate, colon length, and spleen coefficient of TNBS-exposed C57BL/6 mice.
(Fig. 3B and 3C). Histopathological examination of the colon section
revealed evident improvement in inflammatory cell infiltration in PHI
(40 mg/kg) treated colitis mice, compared with the TNBS-treated mice
(Fig. 3D).
Overall, the study provides evidence that PHI has a favorable
pharmaceutical effect in different chemically induced UC models and may
have potential as a therapeutic agent for the treatment of UC.